2. Academic Validation
  3. Further evidence supporting a potential role for ADH1B in obesity

Further evidence supporting a potential role for ADH1B in obesity

  • Sci Rep. 2021 Jan 21;11(1):1932. doi: 10.1038/s41598-020-80563-z.
Liza D Morales 1,  Douglas T Cromack 2,  Devjit Tripathy 2 3,  Marcel Fourcaudot 3,  Satish Kumar 4,  Joanne E Curran 4,  Melanie Carless 5,  Harald H H Göring 4,  Shirley L Hu 6,  Juan Carlos Lopez-Alvarenga 4,  Kristina M Garske 7,  Päivi Pajukanta 7,  Kerrin S Small 8,  Craig A Glastonbury 8,  Swapan K Das 9,  Carl Langefeld 10,  Robert L Hanson 11,  Wen-Chi Hsueh 11,  Luke Norton 3,  Rector Arya 4,  Srinivas Mummidi 4,  John Blangero 4,  Ralph A DeFronzo 2 3,  Ravindranath Duggirala 4,  Christopher P Jenkinson 12
Affiliations

Affiliations

  • 1 South Texas Diabetes and Obesity Institute Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg/Harlingen/Brownsville, TX, USA. liza.morales@utrgv.edu.
  • 2 South Texas Veterans Health Care System, San Antonio, TX, USA.
  • 3 Department of Medicine, University of Texas Health San Antonio, San Antonio, TX, USA.
  • 4 South Texas Diabetes and Obesity Institute Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg/Harlingen/Brownsville, TX, USA.
  • 5 Department of Population Health, Texas Biomedical Research Institute, San Antonio, TX, USA.
  • 6 University of Texas Health Houston, School of Public Health, Brownsville, TX, USA.
  • 7 Department of Human Genetics, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
  • 8 King's College London, London, UK.
  • 9 Internal Medicine-Endocrinology and Metabolism, Wake Forest School of Medicine, Winston-Salem, NC, USA.
  • 10 Department of Biostatistics and Data Science, Wake Forest School of Medicine, Winston-Salem, NC, USA.
  • 11 Phoenix Epidemiology and Clinical Research Branch, NIDDK, Phoenix, AZ, USA.
  • 12 South Texas Diabetes and Obesity Institute Department of Human Genetics, School of Medicine, University of Texas Rio Grande Valley, Edinburg/Harlingen/Brownsville, TX, USA. christopher.jenkinson@utrgv.edu.
PMID: 33479282 DOI: 10.1038/s41598-020-80563-z
Abstract

Insulin is an essential hormone that regulates glucose homeostasis and metabolism. Insulin resistance (IR) arises when tissues fail to respond to Insulin, and it leads to serious health problems including Type 2 Diabetes (T2D). Obesity is a major contributor to the development of IR and T2D. We previously showed that gene expression of alcohol dehydrogenase 1B (ADH1B) was inversely correlated with obesity and IR in subcutaneous adipose tissue of Mexican Americans. In the current study, a meta-analysis of the relationship between ADH1B expression and BMI in Mexican Americans, African Americans, Europeans, and Pima Indians verified that BMI was increased with decreased ADH1B expression. Using established human subcutaneous pre-adipocyte cell lines derived from lean (BMI < 30 kg m-2) or obese (BMI ≥ 30 kg m-2) donors, we found that ADH1B protein expression increased substantially during differentiation, and overexpression of ADH1B inhibited fatty acid binding protein expression. Mature adipocytes from lean donors expressed ADH1B at higher levels than obese donors. Insulin further induced ADH1B protein expression as well as Enzyme activity. Knockdown of ADH1B expression decreased insulin-stimulated glucose uptake. Our findings suggest that ADH1B is involved in the proper development and metabolic activity of adipose tissues and this function is suppressed by obesity.

Figures
Products